ライフサイエンスコーパス: cathepsin B

1 rved in the presence of proteolytic enzymes (cathepsin B).

2 plasma membrane, resulting in the release of Cathepsin B.

3 ing the derepression of the lysomal protease cathepsin B.

4 do not interact with DNA or inhibit protease cathepsin B.

5 chool whiting showed higher activity towards cathepsin B.

6 and lysosomal damage, leading to release of cathepsin B.

7 e (UPR) kinase PERK and the lysosomal enzyme cathepsin B.

8 ion, and by genetic co-deletion of lysosomal cathepsin B.

9 sequent degradation mediated by the protease cathepsin B.

10 e of cathepsin L, including cooperation with cathepsin B.

11 cells from lysosomal breakdown by inhibiting cathepsin B.

12 -ribosylation (ARF)-dependent trafficking of cathepsin B.

13 tem is applied to a screen of inhibitors for cathepsin B.

14 ysteine proteases calpain I, calpain II, and cathepsin B.

15 d subsequent lysosomal damage and release of cathepsin B.

16 active macrophages and the cysteine protease cathepsin B.

17 nt on lysosomal disruption and activation of cathepsin B.

18 VPE activity was independent of cathepsin B.

19 Then, this caused degradation of CTSDmat by cathepsin B.

20 racellular sensing of the lysosomal protease cathepsin B.

21 -expression or pharmacological inhibition of cathepsin B.

22 re located upstream of CTSB, a gene encoding cathepsin B, a cysteine protease involved in keratinocyt

23 e VC(S) linker was designed to be cleaved by cathepsin B, a lysosomal cysteine protease.

24 inhibitor-binding site in cysteine protease cathepsin B, a potential drug target and prognostic mark

25 Cathepsin B abundancy in the model mimicked human diseas

26 as not altered in the cathepsin B mutant and cathepsin B activation was independent of vacuolar proce

27 ty of T-cytotoxic memory cells, which resist cathepsin B activation, may distinguish rejection-free a

28 Tc seemed resistant to cathepsin B activation; (3) with increasing rATG concent

29 ructure of 5-nitro-8-hydroxyquinoline in the cathepsin B active site.

30 Porous silicon nanoneedles can map Cathepsin B activity across normal and tumor human esoph

31 mediated ARF1 inhibition resulted in reduced cathepsin B activity and consequently reduced trypsinoge

32 demonstrate that inhibitors of autophagy or cathepsin B activity and/or molecular targeting of p62/S

33 e-dependent increase in pH and a decrease in cathepsin B activity associated with bacterial survival.

34 It inhibited cathepsin B activity by nearly 40% in vitro.

35 Mice and macrophages lacking cathepsin B activity had increased resistance to the cyt

36 bition of either phagosomal acidification or cathepsin B activity impaired NALP3 activation.

37 The detections of cathepsin B activity in different concentrations of whol

38 to generate LG3 during normoxic conditions, cathepsin B activity was found to be important to genera

39 The same sensor applied to tissue can map Cathepsin B activity with high resolution across the tum

40 vation, blocking ATP signaling, K(+) efflux, cathepsin B activity, and lysosomal acidification all in

41 e oxygen species (ROS) led to an increase in cathepsin B activity, and pharmacological inhibition of

42 Intracellular Ca2+, cytosolic cathepsin B activity, caspase-3 activity, cell viability

43 on pathways was evaluated by studying pH and cathepsin B activity.

44 quires Ad endosomal membrane penetration and cathepsin B activity.

45 abilization (LMP) and subsequent cytoplasmic cathepsin B activity.

46 We show that cathepsin-B activity in the lysosome is upregulated by R

47 f inducible nitric oxide synthase (iNOS) and cathepsin B also reversed chlamydial killing.

48 o used for turn-on fluorescence detection of cathepsin B, an enzyme known to be overexpressed in mamm

49 was shown to increase the release of active cathepsin B, an important matrix remodeling protease.

50 a subsequent caspase 4-dependent cleavage of cathepsin B and a cathepsin B-dependent formation of low

51 Moreover, they are sensitive to proteases (cathepsin B and asparagine endopeptidase) that are over-

52 sium, scavenging mitochondrial ROS, and both cathepsin B and caspase-1 inhibition.

53 Co-expression of cathepsin B and cathepsin B-resistant mutant LFABP in Mc

54 s regulated by a lysosomal pathway, in which cathepsin B and cathepsin D play redundant roles.

55 deficiency in these mice results in enhanced cathepsin B and D activities, indicating lysosomal dysfu

56 Furthermore, the lysosomal protease cathepsin B and HIV-1 induced production of reactive oxy

57 OMK ligands are suitable in vitro probes for cathepsin B and hold promise as a platform to develop mo

58 recruit Bim and Bax to lysosomes to release cathepsin B and induce apoptosis.

59 Cathepsin B and L activities were 90% (+/- SD) [2.4 +/-

60 mography was established, and an increase of cathepsin B and L activity after HP treatment was shown

61 14 +/- 0.08 compared with 0.04 +/- 0.04) and cathepsin B and L expressions in the vastus lateralis of

62 phagic vacuoles and was blocked by lysosomal cathepsin B and L inhibition.

63 unofluorescence assays were used to localize cathepsin B and Lamp2.

64 hese mice express greater amounts of hepatic cathepsin B and lower amounts of liver fatty acid-bindin

65 ERSID is regulated positively by cathepsin B and negatively by PBA1, revealing a complex

66 usion activity triggered by the host factors cathepsin B and Niemann-Pick C1.

67 he expression of critical EBOV entry factors cathepsin B and NPC1.

68 ion were used to investigate the function of cathepsin B and PBA1 in ER-stress-induced PCD (ERSID).

69 L-1beta was also dependent on the release of cathepsin B and production of reactive oxygen species (R

70 lant proteases with caspase-3-like activity, cathepsin B and proteasome subunit PBA1, remains to be e

71 Tibial sections were immunolabeled for cathepsin B and septoclasts were counted.

72 imal cerulein, and the cytosolic activity of cathepsin B and trypsin was evaluated.

73 cretion as compared with cells co-expressing cathepsin B and wildtype LFABP.

74 Activities of cathepsins B and B+L were higher than cathepsin H for al

75 y increasing cathepsin D activity, levels of cathepsins B and D and two proteins known to interact wi

76 to LC3-II conversion, and the activation of cathepsins B and D were assayed with Western blot analys

77 Brain levels of the lysosomal enzymes cathepsins B and D were significantly higher in Npc1-/-

78 nzymes (acid lipase, beta-glucuronidase, and cathepsins B and D).

79 tides were released at the cleavage sites of cathepsins B and D, which thus play an important role.

80 utophagosome-associated lysosomal proteases, cathepsins B and D.

81 hepsin family by RNA interference identified cathepsins B and H as key mediators of TLR3 processing.

82 Given the need for endosomal cathepsins B and L (CatB and CatL) to prime GPs for fusi

83 Caco2 cells were also noted to produce cathepsins B and L, and inhibition of cathepsins suppres

84 ign nevi; we found up-regulation of cysteine cathepsins B and L, matrix metalloproteinase (MMP)-1 and

85 ipating in the processing were identified as cathepsins B and L.

86 n, bromelain, ficin, and mammalian lysosomal cathepsins B and L.

87 specificity relative to rhodesain and human cathepsins B and L.

88 t tumor-associated macrophage (TAM)-supplied cathepsins B and S are critical for promoting pancreatic

89 leavage assays, we demonstrate that cysteine cathepsins B and S can directly cleave Rip1.

90 for Leu-Leu-OMe-induced cell death, whereas cathepsins B and S were required for alum-mediated necro

91 thepsin inhibition and mediated partially by cathepsins B and S.

92 showed that the probe was very selective for cathepsins B and Z, two lysosomal cysteine proteases.

93 Apoptotic (caspase-3+, cathepsin B+) and inflammatory (CD154+) T-cell subsets w

94 ated by blockade of endosomal acidification, cathepsin B, and caspase 1, suggesting that virus intera

95 block proteolytic activities of host furin, cathepsin B, and caspases that mediate toxin's lethality

96 tion, inhibitors of reactive oxygen species, cathepsin B, and K(+) efflux pathways, known to specific

97 lysate spiked with varied concentrations of cathepsin B, and the tissue lysate after immunoprecipita

98 role for the proteolytic cleavage of ENaC by cathepsin B, and we suggest two possible mechanisms by w

99 t of pre-slaughter stress, the activities of cathepsin B- and B/L-like enzymes increased and activiti

100 iple tissues (integrin alpha4/annexin A4 and cathepsin B/apolipoprotein E3) and the other two have a

101 -specific differences in the requirement for cathepsin B are correlated with sequence polymorphisms a

102 we identified a key cell-intrinsic role for cathepsin B as a negative feedback regulator of lysosoma

103 gonorrhoeae activates the cysteine protease cathepsin B as measured by the breakdown of a cathepsin

104 rk further confirmed CDK6, RICTOR, and CTSB (cathepsin B) as targets of miR-218 and examined the func

105 cells apically express the cysteine protease cathepsin B, as indicated by two-dimensional gel electro

106 ysteine protease CPR-4, a homologue of human cathepsin B, as the first RIBE factor in nematodes, to o

107 epsin B within tumor cells, and silencing of cathepsin B attenuated tumor cell invasive capacity in a

108 enzymes with barracouta showing the highest cathepsins B, B+L, D and H activities.

109 This study compared the activities of cathepsins B, B+L, D, H and calpain-like enzymes in crud

110 is hydrolyzable by the proteases plasmin and cathepsin B, both strongly linked with cancer progressio

111 subunit fusion protein was cleaved by active cathepsin B but not the full-length beta or gamma subuni

112 le of trypsin in AP and shows that cytosolic cathepsin B but not trypsin activates cell death pathway

113 Cytosolic cathepsin B but not trypsin activates the intrinsic path

114 pally caspase-dependent to being principally cathepsin B (Cat B)-dependent.

115 istant acid phosphatase histoenzymology, and cathepsin B (CATB) and matrix metalloproteinase 9 (MMP9)

116 iously, we showed that the cysteine protease cathepsin B (CatB) degrades Abeta, most likely by C-term

117 ifically causes a leak of lysosomal protease cathepsin B (CatB) into the cytoplasm.

118 evious work has shown that cleavage of GP by cathepsin B (CatB) is specifically required to generate

119 Cathepsin B (CatB) proteolytically degrades Abeta into n

120 s and angiogenesis are mediated by activated cathepsin B (CatB), a cysteine protease that translocate

121 s inhibitor of cysteine proteases, including cathepsin B (CatB), a recently discovered Abeta-degradin

122 Cathepsin B (cathB) was subsequently confirmed to be dif

123 tophagosome numbers, expression of lysosomal cathepsin B, cathepsin D, Beclin-1, and microtubule-asso

124 after 24 h) by proteolytic enzymes, such as cathepsin B, cathepsin D, prolidase, and plasmin.

125 ent in components of the NLRP3 inflammasome, cathepsin B, cathepsin L or IL-1 molecules.

126 , and either an acid-sensitive bond (1) or a cathepsin B cleavable bond (3) for ensuring an effective

127 Assembling a peptide-based Cathepsin B cleavable sensor over a large array of nano-

128 cers were used in the design: a lysosomally (cathepsin B) cleavable tetrapeptide GFLG spacer conjugat

129 ME27) were tested with endosomal furin- and cathepsin B-cleavable peptide linkers located between th

130 1 activity was assayed following an in vitro cathepsin B cleavage reaction.

131 Whereas cathepsin B cleaved chemokines especially in the C-termi

132 Interestingly, cathepsin B combined with its enzymatic inhibitors led t

133 rs show DNA release by 4 h of treatment with cathepsin B; comparatively, polyplexes formed with pHCat

134 itation showed that there is ~13.4 nM higher cathepsin B concentration in 29.1 microg mL(-1) of whole

135 ate of the endosomal/lysosomal endopeptidase cathepsin B, connected to oligo-(L)-lysine for nucleic a

136 Moreover, cathepsin B contributes to NAIP5/NLRC4 inflammasome-indu

137 sylated and thereby inactivated caspase 3 or cathepsin B could be reactivated through either Trx1- or

138 we suggest two possible mechanisms by which cathepsin B could regulate ENaC.

139 Cathepsin B (CTB) is a cysteine protease believed to be

140 dependent effects of simultaneously deleting cathepsin B (CtsB) and CtsS in a murine pancreatic neuro

141 demonstrate a direct involvement of cysteine cathepsin B (CtsB) and L (CtsL).

142 Cathepsin B (CtsB) contributes to atherosclerosis and ca

143 The lysosomal hydrolase cathepsin B (CTSB) is a known activator of trypsinogen,

144 The cysteine protease cathepsin B (CTSB) is frequently overexpressed in human

145 Cathepsin B (CTSB) is present in both normal and CF epit

146 e intracellular activation of trypsinogen by cathepsin B (CTSB), which can be induced directly via G

147 Cathepsin B (CTSB), which is produced constitutively by

148 Mammalian reoviruses utilize cathepsins B (Ctsb), L (Ctsl), and S (Ctss) for disassem

149 20 purified human thyroglobulin samples with cathepsins B, D, or L, lysosomal proteases that are invo

150 ious findings revealed that ASMase activates cathepsins B/D (CtsB/D), our aim was to investigate the

151 ry CD8(+) T cells was rescued by concomitant cathepsin B deficiency, demonstrating that cathepsin B w

152 However, reports that cathepsin B-deficient macrophages have no defect in part

153 mice treated with a cathepsin inhibitor and cathepsin B-deficient mice suffer limited intestinal inj

154 or four doxorubicin, respectively, through a cathepsin B degradable tetrapeptide linker (-Gly-Phe-Leu

155 Cathepsin B degraded copolymers pHCathK(10) and pHCath(D

156 f rats or mice (wild-type, trypsinogen 7, or cathepsin B-deleted) were stimulated with supramaximal c

157 cies Bundibugyo, containing D47 and I584, is cathepsin B dependent and that ebolavirus Zaire-1995, th

158 se 4-dependent cleavage of cathepsin B and a cathepsin B-dependent formation of low pH intracellular

159 trong association of acinar cell injury with cathepsin B-dependent intracellular activation of trypsi

160 ic deletion or pharmacological inhibition of cathepsin B down-regulated mechanistic target of rapamyc

161 Cathepsin B downregulation reduced reactive oxygen speci

162 sorption capacity, whereas overexpression of cathepsin B enhances fusion.

163 Surprisingly, suppression of cathepsin B expression via CRISPR-Cas9 gene deletion or

164 RNA interference knockdown of cathepsin B expression, however, cannot prevent LT-media

165 calcium binding protein A8 (S100A8), S100A9, cathepsin B, fibronectin, and galectin-3-binding protein

166 uggest that activity-dependent exocytosis of Cathepsin B from lysosomes regulates the long-term struc

167 nterruption of either CCL2-CCR2 signaling or cathepsin B function significantly impaired PNI in vivo

168 ediated knock-down of genes belonging to the cathepsin B gene family.

169 Knock-down of cathepsin B genes reduced aphid fitness, but only on the

170 resulted from greatly increased activity of cathepsins (B>S>L) in venules transitioning into MV, as

171 on of cystatin B, an endogenous inhibitor of cathepsins B, H and L, on the development of NPC neuropa

172 Now, a chemiluminescent probe for cathepsin B has been developed that provides a 16,000-fo

173 Human cathepsin B has many house-keeping functions, such as pr

174 ntial role of cytosolic trypsin vs cytosolic cathepsin B in activation of apoptosis.

175 metastasis to bone that is coexpressed with cathepsin B in bone metastases.

176 sefulness against the deleterious effects of cathepsin B in cancer progression.

177 indings established a prometastatic role for cathepsin B in distant metastasis and illustrated the th

178 ified the activity of the lysosomal protease cathepsin B in macrophages as a rate-limiting factor in

179 siRNA-mediated knockdown of cathepsin B in McA-RH7777 cells resulted in a 39% increa

180 f their possible target enzymes legumain and cathepsin B in MDA-MB-435S, A375, and C8161 melanoma cel

181 ntified a fundamental biological function of cathepsin B in providing a checkpoint for homeostatic ma

182 ion of CTSB, as well as stronger staining of cathepsin B in the stratum granulosum of affected indivi

183 ction and therapeutic targeting potential of cathepsin B in this setting of advanced disease.

184 RNA interference-mediated knockdown of cathepsin B in tumor cells reduced collagen I degradatio

185 ting the ability to effectively label active cathepsin B in vitro.

186 Finally, cathepsin B inactivation protected mitochondria, decreas

187 Cathepsin B increased the activity of matrix metalloprot

188 Purified lysosomal enzymes, specifically cathepsin B, inhibited cryptococcal growth.

189 Sensitivity to chloroquine, cathepsin B inhibition, and a G-rich inhibitory oligodeo

190 escence, AlphaLISA, and enzymatic assays for cathepsin B inhibition.

191 oneal administration of the highly selective cathepsin B inhibitor CA-074 reduced metastasis in tumor

192 activity decreases with the application of a cathepsin B inhibitor directly onto the apical side of 2

193 Prior studies have found that the cathepsin B inhibitor, Ca074Me, suppresses this response

194 CA-074Me, a potent cathepsin B inhibitor, protects LT-sensitive macrophages

195 Taking advantage of previous studies of cathepsin B inhibitor-resistant viruses, we found that v

196 r, lysosomal acidification inhibitors, and a cathepsin B inhibitor.

197 Further, treatment of normal cells with cathepsin B inhibitors during the differentiation proces

198 structure-based design and synthesis of new cathepsin B inhibitors using the cocrystal structure of

199 on of lysosomal membranes and the release of cathepsin B into the cytoplasm are required for Ad-induc

200 ut not ts1, induces the release of lysosomal cathepsin B into the cytoplasm of infected cells.

201 Finally, excessive release of cathepsin B into the cytosol can lead to cell death thro

202 proteins Bim and Bax to lysosomes, releasing cathepsin B into the cytosol where it mediates mitochond

203 sted particles disrupt lysosomes and release cathepsin B into the cytosol, somehow activating NLRP3.

204 ite for AP only because it causes release of cathepsin B into the cytosol.

205 teolytic activity of a cancer-related enzyme cathepsin B is measured with alternating current voltamm

206 Intracellular activity of cathepsin B is significantly enhanced at the onset of os

207 Cathepsin L, but not cathepsin B, is an important contributor in this process

208 release of the lysosomal cysteine proteases cathepsin B, K, L, and S and that was independent of the

209 h inhibits the cysteine proteases papain and cathepsins B, K and L up to 2 times more potently than 1

210 ated that it was a potent inhibitor of human cathepsins B, K, and L ( Ki = 6.87, 0.49, and 0.34 nM, r

211 nd non-ELR (CXCL9-12) chemokines by cysteine cathepsins B, K, L, and S at neutral pH by high resoluti

212 lectivity toward cathepsin L than papain and cathepsins B, K, V, and S with no activity against cathe

213 The cathepsin B knockdown and 24-h treatment with OA resulte

214 Cathepsin B knockdown was accompanied by a 74% increase

215 Cathepsin B-knockout mice and wild-type animals were pla

216 ated with texture (r(2) = 0.4), as also were cathepsin B&L and sex.

217 ling and tiger flathead demonstrated higher cathepsin B+L activity, whereas gemfish and eastern scho

218 The cathepsin B+L and B activities increased significantly w

219 Collectively, these data indicate that cathepsins B, L, and S influence reovirus pathogenesis a

220 macrophages, singly or multiply deficient in cathepsins B, L, C, S and X.

221 Pharmacological inhibition of cathepsin B/L enhanced EPO-induced red cell formation in

222 phagosomes and late endosomes to SiNP-filled cathepsin B/L-containing lysosomes rather than elevated

223 Spi2A defects were ameliorated by cathepsin-B/L inhibition, and by genetic co-deletion of

224 The mRNA levels of cathepsins B/L and plasminogen activators, but not MMPs,

225 testing inhibitors of TGF-beta signaling and cathepsins B/L in the therapy of invasive/metastatic mel

226 ted by cell membrane-permeable inhibitors of cathepsins B/L, but not by wide-spectrum inhibitors of M

227 y monocytes, and inhibition of phagocytosis, cathepsin B leakage, generation of reactive oxygen speci

228 n vivo studies have suggested that during AP cathepsin B leaks into the cytosol from co-localized org

229 Reducing cathepsin B levels via siRNA following TNFalpha exposure

230 Recent studies have shown that a cathepsin B like protease, TbcatB, is essential to the s

231 te that inhibition of the lysosomal protease cathepsin b-like blocks endocytosis, causing cell death.

232 can be attributed to inhibition of lysosomal cathepsin b-like protease activity.

233 RNA interference studies implicated a cathepsin B-like protease, tbcatB, as a key inhibitor ta

234 namic activities of aleurain-like proteases, cathepsin B-like proteases, and vacuolar processing enzy

235 otease subfamilies: aleurain-like proteases, cathepsin B-like proteases, and vacuolar processing enzy

236 ed by a direct activity assay of recombinant cathepsin b-like protein.

237 Cathepsin B may cleave ENaC extracellularly after being

238 Cathepsin B may execute its function after tonoplast rup

239 that multiple redundant cathepsins (not just cathepsin B) mediate this process by evaluating IL-1beta

240 Cathepsin B-mediated CD18 shedding regulates leukocyte r

241 tes joint inflammation in arthritis, induces cathepsin B-mediated cleavage of SirT1, resulting in red

242 clast precursor fusion and that a temporary, cathepsin B-mediated decrease in myosin IIA levels trigg

243 ages and potentiate nerve invasion through a cathepsin B-mediated process.

244 The prototype for this phenomenon is cathepsin B-mediated trypsin generation.

245 the maturation of autophagosomes results in cathepsin B-mediated trypsinogen activation induced by c

246 Using the system, a label-free screen for cathepsin B modulators against 1280 chemicals was comple

247 Tonoplast rupture was not altered in the cathepsin B mutant and cathepsin B activation was indepe

248 gen, such as trypsinogen-7-null (T(-/-)) and cathepsin B-null (CB(-/-)) mice, have been used to study

249 ogenesis was reduced by approximately 50% in cathepsin B-null mice.

250 initial increase in cytoplasmic activity of cathepsin B occurs at the same time or shortly before ca

251 , or NLRP3 deficiency, but are unaffected by cathepsin B or caspase-1 inhibitors.

252 ncreases the activity of cathepsin D but not cathepsins B or L.

253 ytosol and genetic suppression of caspase 4, cathepsin B, or apoptosis-inducing factor function signi

254 However, discovering probes selective to cathepsin B over other cysteine cathepsins is a signific

255 rm organization of autophagosomes as well as cathepsin B overactivity).

256 s and shRNA-mediated depletion, we show that cathepsin B participates in podosomes-mediated focal mat

257 appears, as is the case of C99, in enlarged cathepsin B-positive structures, while extracellular Abe

258 stigated the subcellular distribution of the cathepsin B precursor, procathepsin B.

259 and secreted proteins, including Tenascins, Cathepsin-B precursor, cystatin, and numerous Variant-sp

260 ic groups to generate a library of candidate cathepsin B probes.

261 he specific proteolysis of the Fc-peptide by cathepsin B produces decay in the ACV peak current versu

262 studies in human specimens demonstrated that cathepsin B-producing macrophages were enriched in invad

263 Herein, we show that T. gondii cathepsin B protease (TgCPB) does not undergo self-matur

264 lithography show a much faster kinetics for cathepsin B proteolysis with kcat/KM = 9.2 x 10(4)M(-1)s

265 whereas several specific inhibitors against cathepsin B, reactive oxygen species, or ubiquitin-media

266 Lysosomal permeabilization and cathepsin B redistribution into the cytoplasm occurred s

267 y, and pharmacological inhibition of ROS and cathepsin B reduced iNOS expression.

268 Finally, cathepsin B regulated TGF-beta production/signaling, whi

269 Together, these data indicate that cathepsin B regulates VLDL secretion and free fatty acid

270 tion of either lysosomal Ca(2+) signaling or Cathepsin B release prevented the maintenance of dendrit

271 omal Zn, which activated lysosomal swelling, cathepsin B release, and LCD.

272 potassium flux, lysosomal acidification, and cathepsin B release.

273 Co-expression of cathepsin B and cathepsin B-resistant mutant LFABP in McA-RH7777 cells r

274 molecular targeting of p62/SQSTM1, Atg7, or cathepsin B result in partial reversal of the suppressiv

275 Overexpression of cathepsin B resulted in decreased OA uptake and VLDL sec

276 fied alphabetaI with the cysteine proteinase cathepsin B results in the specific proteolysis of the H

277 The septoclast is a specialized, cathepsin B-rich, perivascular cell type that accompanie

278 -induced IL-1beta generation have questioned cathepsin B's involvement.

279 SIRT1 is an important substrate of cysteine cathepsins B, S, and L.

280 Inhibition of cathepsin B shows that this protease is an apical contro

281 Cathepsin B small interfering RNA (siRNA) was transfecte

282 A cathepsin B-specific cleavable substrate (KGRR) conjugat

283 athepsin B as measured by the breakdown of a cathepsin B substrate.

284 The Trypanosoma brucei cysteine protease cathepsin B (TbCatB), which is involved in host protein

285 f primary melanomas and benign nevi revealed cathepsin B to be predominantly expressed by melanoma ce

286 erved with other proteases such as thrombin, cathepsin B, tryptase, and tissue plasminogen activator.

287 CmCatB, a cathepsin B-type cysteine protease, is insensitive to in

288 through impairing the proteolytic cascade of cathepsin B/urokinase-type plasminogen activator (uPA)/m

289 t cathepsin B deficiency, demonstrating that cathepsin B was a physiological target of Spi2A in memor

290 formation of low pH intracellular vesicles; cathepsin B was activated and released into the cytosol

291 Cathepsin B was identified as the TNFalpha-responsive pr

292 Co-localization of LFABP and cathepsin B was observed in a distinct Golgi apparatus-l

293 .68 +/- 0.50) x 10(4)M(-1)s(-1) for purified cathepsin B was obtained.

294 The lysosomal protease cathepsin B was required for IL-1beta release but not pr

295 Activity of the lysosomal protease cathepsin B was suppressed by genetic and pharmacologica

296 in neuronal media, and both cathepsin L and cathepsin B were demonstrated to be important for increa

297 Transcript level and activity labelling of cathepsin B were used to assess activation.

298 ies of Th subsets, which expressed activated cathepsin B, were similarly increased with combined stim

299 and Cote d'Ivoire are strongly dependent on cathepsin B, while the ebolaviruses Sudan and Reston and

300 ndent down-regulation of the matrix protease cathepsin B within tumor cells, and silencing of catheps